《Plasticity》
Bluelight Crew
- Joined
- Sep 21, 2013
- Messages
- 3,115
That's it? That's your response? Easy to cop out when you completely ignore and fail to respond to the post at hand, but it kinda shows your cards I guess. Since the OP gave me the greenlight I'll bite
. You made an unjust claim and touted it as fact, so I asked for you to back up your claim. Instead you decided to spout out whatever you could, even false information to avoid giving a source on your claim so I voiced not only my opinion, but general, rather common knowledge that would debunk some claims you made, I say "claims" because not even you knew what you were claiming... naming shit like "serotonin agonist" "wait serotonin antagonist" "no, SSRI/SNRI" and then to just "SNRI".
Examples of the common knowledge I speak of is the downregulation at 5-ht2a if kratom were to truely contain any 5-ht2a antagonists and the complete lack of any serotonin syndrome occuring from an kratom and MAOI consumption, as well as the lack of negative interaction associated with kratom in conjuction with most classes of drugs which would be potentially deadly if kratom "works on serotonin just like tramadol". If kratom worked on serotonin in the same way as tramadol, why aren't there more people than just the handfull dropping dead from kratom combos? It's certainly more popular then it ever was...
Remember who was the one who made the claim, if logic just happens to question or possibly even debunk your claim altogether then be prepared to provide evidence for your claim, not false information (the fake deaths) and personal anectdote that doesn't fall in line with most, if not all kratom users (the SSRI withdrawals from kratom). By your logic, I might as well go ahead attributing pharmocological profiles to poorly understood drugs because it hasn't been proven.
From henceforth I now declare gabapentin, a dopamine agonist with potentially dangerous 5-ht2b activity, and let's go ahead and throw some psychedelic activity at 5-ht2a.... you know, until it's debunked for good
. Probably can be, so possible poor example, but you get the jest... now if you will excuse me, I may now proceed to enjoy my steak...

Examples of the common knowledge I speak of is the downregulation at 5-ht2a if kratom were to truely contain any 5-ht2a antagonists and the complete lack of any serotonin syndrome occuring from an kratom and MAOI consumption, as well as the lack of negative interaction associated with kratom in conjuction with most classes of drugs which would be potentially deadly if kratom "works on serotonin just like tramadol". If kratom worked on serotonin in the same way as tramadol, why aren't there more people than just the handfull dropping dead from kratom combos? It's certainly more popular then it ever was...
Remember who was the one who made the claim, if logic just happens to question or possibly even debunk your claim altogether then be prepared to provide evidence for your claim, not false information (the fake deaths) and personal anectdote that doesn't fall in line with most, if not all kratom users (the SSRI withdrawals from kratom). By your logic, I might as well go ahead attributing pharmocological profiles to poorly understood drugs because it hasn't been proven.
From henceforth I now declare gabapentin, a dopamine agonist with potentially dangerous 5-ht2b activity, and let's go ahead and throw some psychedelic activity at 5-ht2a.... you know, until it's debunked for good
